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首页> 外文期刊>Nature >Embolus extravasation is an alternative mechanism for cerebral microvascular recanalization
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Embolus extravasation is an alternative mechanism for cerebral microvascular recanalization

机译：栓子外渗是脑微血管再通的另一种机制

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摘要

Cerebral microvascular occlusion is a common phenomenon throughout life that might require greater recognition as a mechanism of brain pathology. Failure to recanalize microvessels promptly may lead to the disruption of brain circuits and significant functional deficits. Haemodynamic forces and the fibrinolytic system are considered to be the principal mechanisms responsible for recanalization of occluded cerebral capillaries and terminal arterioles. Here we identify a previously unrecognized cellular mechanism that may also be critical for this recanalization. By using high-resolution fixed-tissue microscopy and two-photon imaging in living mice we observed that a large fraction of micro-emboli infused through the internal carotid artery failed to be lysed or washed out within 48 h. Instead, emboli were found to translocate outside the vessel lumen within 2-7 days, leading to complete re-establishment of blood flow and sparing of the vessel. Recanalization occurred by a previously unknown mechanism of microvascular plasticity involving the rapid envelopment of emboli by endothelial membrane projections that subsequently form a new vessel wall. This was followed by the formation of an endothelial opening through which emboli translocated into the perivas-cular parenchyma. The rate of embolus extravasation was significantly decreased by pharmacological inhibition of matrix metalloproteinase 2/9 activity. In aged mice, extravasation was markedly delayed, resulting in persistent tissue hypoxia, synaptic damage and cell death. Alterations in the efficiency of the protective mechanism that we have identified may have important implications in microvascular pathology, stroke recovery and age-related cognitive decline.
机译：脑微血管闭塞是一生中的常见现象，可能需要作为脑病理学的一种机制而得到更大的认可。未能及时重新穿通微血管可能会导致脑回路破裂和明显的功能缺陷。血流动力学力和纤溶系统被认为是导致闭塞性脑毛细血管和末梢小动脉再通的主要机制。在这里，我们确定了以前无法识别的细胞机制，这对于再次通气也可能至关重要。通过在活着的小鼠中使用高分辨率固定组织显微镜和双光子成像，我们观察到通过颈内动脉注入的大部分微栓子在48小时内没有被溶解或冲洗掉。取而代之的是，发现栓子在2至7天内转移到血管腔外部，从而导致血流完全恢复和保留血管。血管再通是通过微血管可塑性的一种先前未知的机制发生的，该机制涉及通过随后形成新的血管壁的内皮膜突出物快速包埋栓子。随后形成内皮开口，栓子通过内皮开口移位进入血管周围薄壁组织。药理学抑制基质金属蛋白酶2/9活性可显着降低栓子外渗的速率。在老年小鼠中，外渗明显延迟，导致持续的组织缺氧，突触损伤和细胞死亡。我们已经确定的保护机制效率的改变可能对微血管病理学，中风恢复和与年龄有关的认知能力下降具有重要意义。

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  • 来源
    《Nature》 |2010年第7297期|p.478-482|共5页
  • 作者

    Carson K. Lam; Taehwan Yoo; Bennett Hiner; Zhiqiang Liu; Jaime Grutzendler;

  • 作者单位

    Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Ilinois 60611 USA;

    Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Ilinois 60611 USA;

    Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Ilinois 60611 USA;

    Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Ilinois 60611 USA;

    Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, Ilinois 60611 USA Physiology, Northwestern University Feinberg School of Medicine, Chicago, Ilinois 60611, USA;

  • 收录信息 美国《科学引文索引》(SCI);美国《工程索引》(EI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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